Necdin enhances muscle reconstitution of dystrophic muscle by vessel-associated progenitors, by promoting cell survival and myogenic differentiation

P. Pessina, V. Conti, R. Tonlorenzi, T. Touvier, R. Meneveri, G. Cossu, S. Brunelli

Research output: Contribution to journalArticle

Abstract

Improving stem cell therapy is a major goal for the treatment of muscle diseases, where physiological muscle regeneration is progressively exhausted. Vessel-associated stem cells, such as mesoangioblasts (MABs), appear to be the most promising cell type for the cell therapy for muscular dystrophies and have been shown to significantly contribute to restoration of muscle structure and function in different muscular dystrophy models. Here, we report that melanoma antigen-encoding gene (MAGE) protein necdin enhances muscle differentiation and regeneration by MABs. When necdin is constitutively overexpressed, it accelerates their differentiation and fusion in vitro and it increases their efficacy in reconstituting regenerating myofibres in the α-sarcoglycan dystrophic mouse. Moreover, necdin enhances survival when MABs are exposed to cytotoxic stimuli that mimic the inflammatory dystrophic environment. Taken together, these data demonstrate that overexpression of necdin may be a crucial tool to boost therapeutic applications of MABs in dystrophic muscle.

Original languageEnglish
Pages (from-to)827-838
Number of pages12
JournalCell Death and Differentiation
Volume19
Issue number5
DOIs
Publication statusPublished - May 2012

Keywords

  • apoptosis
  • muscle dystrophy
  • necdin
  • stem cells

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

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